As has often been pointed out in these blog posts, the "evidence" offered by Discovery Institute fellows William A. Dembski and Michael J. Behe for an intelligent designer can, by the same logic and using the same evidence, be interpreted as pointing to a theologically awkward malevolent designer. This is a line of reasoning routinely ignored by the "Cdesign proponentcists", who prefer to overlook the many examples of parasites and pathogens—and the evolutionary traits that make them so successful at invading and surviving within their hosts.
A fresh example that creationists will either have to ignore or blame on "The Fall" comes from researchers at the Leibniz Institute for Natural Product Research and Infection Biology. They have shown that the fungus Candida albicans, which causes thrush, has evolved a highly sophisticated and "finely tuned" mechanism for infecting the human mouth while evading the immune system.
The stock creationist response is to shift responsibility onto the biblical myth of "The Fall," retreating into Bible literalism. Yet this is precisely the kind of literalism the Discovery Institute has been at pains to insist is not essential to the notion of intelligent design, which it markets as a scientific alternative to evolutionary theory—or "Darwinism," as they prefer to call it. This rhetorical sleight of hand was central to the Institute’s "Wedge Strategy," devised after the 1987 US Supreme Court ruling in Edwards v. Aguillard, which confirmed that teaching creationism in public schools violated the Establishment Clause of the First Amendment.
The new research reveals that C. albicans produces a toxin called candidalysin in carefully regulated doses that allow it to infiltrate the mucous lining of the mouth. Too little candidalysin, and the fungus would fail to establish itself; too much, and it would trigger an immune response strong enough to destroy it. Normally, C. albicans exists in a round, yeast-like form, but under the "right" conditions it can switch into the filamentous hyphal form typical of fungi. This transformation allows it to penetrate host tissues and, in immune-compromised patients, become life-threatening. It is in this invasive hyphal state that C. albicans produces candidalysin.
The production of hyphae, and therefore candidalysin, is controlled by the gene EED1. By any definition, EED1 would qualify as an example of "complex specified information" according to Dembski’s own formulation — evidence, according to the Discovery Institute, of supernatural intelligent design.
Background: Origins of Candida albicans.This discovery is detailed in an open-access paper in Nature Microbiology and a Leibniz-Hans Knoell Institute (HKI) news release by Friederike Gawlik.
- Taxonomic position: Candida albicans is a fungus in the phylum Ascomycota, class Saccharomycetes, closely related to baker’s yeast (Saccharomyces cerevisiae). It belongs to the CUG clade, a group of yeasts notable for reassigning the genetic codon CUG to code for serine instead of leucine—a highly unusual evolutionary development.
- Commensal origins: C. albicans is thought to have originated as a harmless commensal organism living in the guts and mucosal surfaces of warm-blooded animals. It is normally part of the human microbiota, colonising the mouth, gut, and genital tract without causing disease in healthy individuals.
- Opportunistic pathogen: Its pathogenicity likely arose as a by-product of its commensal lifestyle. When host defences are weakened, or when the microbiome balance is disturbed, C. albicans can switch to a filamentous (hyphal) form, invade tissues, and cause disease. This dimorphic switch is considered a key evolutionary adaptation, allowing it to survive both as a benign coloniser and as an opportunistic pathogen.
- Ancient lineage: Molecular phylogenetics suggests Candida species diverged from their yeast relatives tens of millions of years ago, long before humans appeared. Its evolution has been shaped by coexistence with vertebrate hosts, with the ability to tolerate and exploit the mammalian immune system emerging gradually through natural selection.
- Genetic diversity: Unlike many fungi, C. albicans does not have a well-defined sexual cycle, but it maintains genetic diversity through parasexual reproduction, in which diploid cells undergo chromosome loss after cell fusion. This unusual system helps it adapt rapidly to new environments—including antimicrobial pressures.
Does it have host-specific varieties?
Good question. Yes—Candida albicans does show signs of host specificity, though not in the strict sense of being divided into completely separate subspecies. Here’s the state of knowledge: Host-Specific Varieties of Candida albicans
- Broad host range: C. albicans is primarily a human commensal and pathogen, but it can also colonise and infect other mammals, including mice, dogs, cats, and non-human primates.
- Genetic diversity: Population genomics has shown that C. albicans strains are highly diverse, with some degree of host-associated clustering. Certain lineages appear to be better adapted to humans, while others are found more frequently in non-human animals.
- No strict subspecies: Unlike some other pathogens, C. albicans has not split into distinct, host-specific subspecies. Instead, it maintains a flexible genome that allows it to adapt to different hosts and niches.
- Strain variation in virulence: Different strains show variations in virulence traits—such as the ability to form hyphae, secrete toxins like candidalysin, or evade immune responses—which may reflect adaptations to particular host environments.
- Other Candida species: In contrast, some of its close relatives do show more marked host preferences. For example, Candida dubliniensis is almost exclusively found in humans, whereas Candida tropicalis is widespread in both humans and animals.
So the answer is: C. albicans itself doesn’t have clearly defined host-specific varieties, but it exhibits a great deal of genetic and phenotypic flexibility, allowing it to infect multiple species. Its adaptability is a hallmark of its evolutionary success.
The dose makes the difference
Candida albicans produces a toxin that causes illness – but in small amounts, it helps the fungus to survive permanently in the oral mucosa
The yeast fungus Candida albicans not only uses the toxin candidalysin to cause infections, but also to colonize the oral mucosa inconspicuously – but only in finely balanced amounts. Too little toxin prevents oral colonization, too much triggers the immune system and leads to an inflammatory defense reaction, as an international research team from Zurich, Jena, and Paris discovered. The results were published in the journal Nature Microbiology.
Candida albicans is a yeast fungus that occurs naturally in the human microbiome and usually remains harmless. Under certain conditions, however, it can transform from its round yeast form into thread-like hyphae and cause infections that can have fatal consequences, especially in immunocompromised patients. In this hyphal form, Candida albicans produces the toxin candidalysin, a protein that directly attacks host cells.
We knew that the fungal toxin candidalysin can cause disease. What is new is that it is also necessary for the fungus to survive in the mouth. The yeast fungus Candida albicans uses the toxin like a door opener to anchor itself in the mucous membrane. As long as it only produces it in small quantities, it remains under the radar of the immune system and survives in the oral cavity in the long term.
Professor Bernhard Hube, co-corresponding author
Department of Microbial Pathogenicity Mechanisms
Leibniz Institute for Natural Product Research and Infection Biology–Hans Knoell Institute (HKI)
Jena, Germany.
To clarify this connection, an international team worked with mouse models. Researchers led by Salomé LeibundGut-Landmann at the University of Zurich showed how the immune system reacts to different fungal strains. The Leibniz-HKI in Jena contributed investigation into the genetic basis: the team used targeted interventions to modify genes that control hyphae formation and toxin production in the yeast fungus. Researchers at the Institut Pasteur in Paris then used bioinformatic analysis to orient the genetic information in an evolutionary context.
Two very different Candida strains were compared: The aggressive laboratory strain SC5314 forms long hyphae and produces large amounts of candidalysin. As a result, the immune system reacts immediately with severe inflammation and eliminates the fungus after a short time. Strain 101, which occurs naturally in the mouth, behaves very differently: it produces only small amounts of the toxin and can thus remain inconspicuous in the mucous membrane without triggering a strong immune response.
The fungus drives with the handbrake on, so to speak. It needs a little toxin, but too much is immediately punished.
Professor Bernhard Hube.
It is precisely these differences between the strains that show how important the fine regulation of candidalysin is for colonizing different niches in the body. Only if Candida albicans finds the correct amount, then the fungus can survive in the mouth long-term without being fought by the immune system.
Dr. Tim B. Schille, co-author.
Department of Microbial Pathogenicity Mechanisms
Leibniz Institute for Natural Product Research and Infection Biology–Hans Knoell Institute (HKI)
Jena, Germany.
The gene EED1 also plays a key role in this process. It regulates hyphae formation and thus indirectly influences the production of candidalysin. This allows the fungus to remain largely unnoticed in the oral mucosa. However, if this balance is upset, infections can develop.
It is remarkable how well the fungus regulates its activity. This balance also explains why the toxin has been preserved evolutionarily: it enables the fungus to live permanently in the oral mucosa, but at the same time makes it dangerous as a potential pathogen.
Dr. Tim B. Schille.
The study shows that candidalysin may be an important factor in the colonization of certain areas of the body by Candida yeasts. So far, the results have only yielded cautious prospects for medicine.
We cannot yet derive any therapeutic applications for oral Candida infections. In the case of vaginal infections, however, we have already been able to show in earlier studies that the toxin can be neutralized. This can significantly reduce tissue damage caused by Candida albicans, which is typical of vaginal yeast infections.
Professor Bernhard Hube.
The project was initiated and coordinated by researchers in Zurich, with significant participation from the Leibniz-HKI in Jena and the Institut Pasteur in Paris. The study was funded by the German Research Foundation (DFG) as part of the Cluster of Excellence ‘Balance of the Microverse’ at Friedrich Schiller University Jena and the Collaborative Research Center/Transregio 124 (FungiNet)‘. Publication:
Abstract
Candida albicans is a common fungal member of the human microbiota but can also cause infections via expression of virulence factors associated with the yeast-to-hyphae transition. The evolutionary selection pressure to retain these pathogenic traits for a commensal microorganism remains unclear. Here we show that filamentation and hyphae-associated factors, including the toxin candidalysin, are crucial for colonization of the oral cavity, a major reservoir of C. albicans. Low-virulent strains of C. albicans expressed the candidalysin-encoding gene ECE1 transiently upon exposure to keratinocytes in vitro. In mice, ECE1 mutants were defective at accessing terminally differentiated oral epithelial layers where the fungus is protected from IL-17-mediated immune defence. Tight regulation of ECE1 expression prevented detrimental effects of candidalysin on the host. Our results suggest that hyphae-associated factors such as candidalysin govern not only pathogenicity, but also mucosal colonization through direct host interactions enabling C. albicans to create and maintain its niche in the oral mucosa.
Main
Microorganisms colonizing human epithelial tissues are crucial for maintaining and modulating host barrier homeostasis and physiology. While microbiome research has primarily focused on bacteria, recent studies underscore the beneficial effects of commensal fungi for the host. Candida albicans can enhance resistance to infections via the induction of type 17 immunity1,2,3. Yet, C. albicans is also a pathobiont causing mucosal infections4,5. Furthermore, C. albicans can cause life-threatening systemic disease6 and is implicated in non-infectious chronic inflammatory disorders, including inflammatory bowel disease, hepatitis and airway allergies2,7,8,9. These opposing roles emphasize the importance of understanding how C. albicans maintains a balanced homeostatic relationship with its host.
Several studies suggest that the yeast morphology and repression of hyphae-associated genes are required for C. albicans gut colonization, while hyphal growth and associated factors are linked to pathogenicity3,10. Such a scenario would favour avirulent strains3. However, most clinical isolates of C. albicans retain considerable virulence potential11, raising the question why such traits have been conserved. One explanation is that hyphae may also play non-pathogenic roles during colonization12,13. In fact, hyphal formation and candidalysin—a hypha-associated peptide toxin encoded by the ECE1 gene and known to damage epithelial barriers and trigger inflammation14,15—have been shown to support gut colonization by inhibiting competing bacteria16.
Beyond the gut, C. albicans also inhabits the oral cavity, a potential primary reservoir for fungal colonization11,17. The oral mucosa, with its cornified stratified epithelium and continuous exposure to environmental stimuli, differs markedly from the gut and presents unique colonization challenges18. Unlike in the gut, where C. albicans is found in the lumen10,16, in the oral mucosa it resides within the uppermost layer of the stratified epithelium19,20. However, the fungal factors supporting stable colonization in this niche are not well defined.
Here we show that C. albicans relies on filamentation and candidalysin to establish and maintain oral colonization. In this process, candidalysin can breach the stratum corneum supporting growth and immune evasion without host adverse effects. These findings suggest that classical virulence traits have evolved not primarily for pathogenicity but to promote stable mucosal colonization.
Fróis-Martins, R., Lagler, J., Schille, T.B. et al.
Dynamic expression of candidalysin facilitates oral colonization of Candida albicans in mice.
Nat Microbiol (2025). https://doi.org/10.1038/s41564-025-02122-4
Copyright: © 2025 The authors.
Published by Springer Nature Ltd. Open access.
Reprinted under a Creative Commons Attribution 4.0 International license (CC BY 4.0)
Of course, if one insists on seeing the hand of a designer in this “finely tuned” mechanism, the obvious question is why such an entity would go to the trouble of engineering a fungus capable of causing so much human suffering. The theology becomes awkward at this point since the evidence often looks more like malevolent design than benevolent design.
Evolution, by contrast, makes the picture both simpler and more coherent. Candida albicans did not arise to cause disease, nor was it designed to torment humans; it is a long-standing commensal organism that happens, under certain conditions, to cross the line into pathogenicity. Its toxin production, hyphal growth, and immune evasion are best understood as the result of gradual refinements that allowed it to balance survival with host tolerance. In other words, what looks like “design” is nothing more than natural selection fine-tuning survival strategies over millions of years.
It speaks to the unscientific nature of intelligent design creationism that much of the evidence must either be ignored or explained away with unproven religious mythology and appeals to the supernatural. Science, by contrast, accommodates all observations within a coherent, logical, and testable framework — and when new evidence emerges, it refines and improves that explanation accordingly.
This is the recurring problem for creationists and “intelligent design” advocates: if the evidence they cite truly points to purposeful engineering, then that purpose appears cruel, capricious, and wholly at odds with the benevolent deity they wish to defend. Evolutionary biology, on the other hand, explains the same evidence without recourse to supernatural intent — malevolent or otherwise.
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